Probiotic yeast Saccharomyces boulardii exerts direct probiotic action on pathogenic E. coli by trapping them on surfaces and inactivating toxic lipopolysaccharides. Using optical dark-field microscopy, we show that nonpathogenic E. coli cells also readily bind probiotic S. boulardii. More importantly, the adhered nonpathogenic E. coli progressively damage S. boulardii cell walls and lyse them. Co-cultured methylene blue-supplemented agar-plate assay indicates that rough lipopolysaccharides might be playing a key role in S. boulardii cell wall damage. When experiments are repeated with lipopolysaccharide-depleted E. coli and also lipopolysaccharide-deficient E. coli, adhesion decreases substantially. The co-cultured assay further reveals that free lipopolysaccharides, released from E. coli, are also causing damage to S. boulardii walls like adhered E. coli. These new findings contradict the known S. boulardii-E. coli interaction mechanisms. We confirm that E. coli cells do not bind or damage human erythrocyte cell walls; therefore, they have not developed pathogenicity. The combined results demonstrate the first example of nonpathogenic E. coli being harmful to probiotic yeast S. boulardii. This finding is important because gut microbial flora contain large numbers of nonpathogenic E. coli. If they bind or damage probiotic S. boulardii cell walls, then the probiotic efficiency toward pathogenic E. coli will be compromised.
Keywords: cell wall damage; dark-field microscopy; drug-resistance and pathogenicity; lipopolysaccharides; live cell imaging.